Propofol decreases cerebral metabolic rate for oxygen and cerebral blood flow. By causing vasoconstriction of central nervous system (CNS) blood vessels, propofol also significantly decreases intracranial pressure.
Propofol produces a dose-dependent decrease in ventilatory drive. It decreases tidal volume and minute ventilation and increases Paco2. The ventilatory depressant effect is exaggerated in patients with underlying chronic obstructive pulmonary disease (COPD).
Propofol decreases myocardial contractility, leading to a reduction in cardiac output. It reduces smooth muscle tone, causing vasodilation in both systemic arteries and veins. Propofol also blunts the barostatic reflex, resulting in a slower heart rate for a given decrease in blood pressure.
Coexisting factors, such as other medications (eg, benzodiazepines and/or opioids), advanced age, or presence of concurrent disease (eg, cardiac dysfunction, COPD, hypovolemia), can increase the hemodynamic effects of propofol and decrease the amount needed to produce unconsciousness. Patients with acquired tolerance because of chronic use of other CNS depressants, anticonvulsants, or alcohol may require higher doses of propofol to produce unconsciousness.
Propofol causes the lowest incidence of postoperative nausea and vomiting of any general anesthetic agent, injected or inhaled. Propofol also has intrinsic antiemetic activity and has been used successfully as an antiemetic.
Propofol often causes pain on injection, which can sometimes be severe. Placing a tourniquet proximal to the injection site and administering lidocaine is the most effective way to prevent this pain.
Propofol is a very short-acting intravenous anesthetic. It undergoes relatively little accumulation, even after long-duration infusions. Because of its rapid recovery characteristics, it is an extremely useful drug for maintaining general anesthesia.
Fospropofol is a new, water-soluble prodrug of propofol. The onset of the sedative effect is slow.
The CNS effects of thiopental are qualitatively similar to those of propofol. When thiopental is given before a planned decrease in global cerebral perfusion, the likelihood of CNS damage appears to be reduced.
The cardiac and pulmonary effects of thiopental are qualitatively similar to those of propofol. Thiopental generally causes a smaller decrease in blood pressure.
The CNS effects of etomidate are similar to those of thiopental and propofol.
Etomidate is notable for its lack of cardiovascular effects. Given by itself, it has little effect on systemic arterial or venous vascular tone or on cardiac contractility, and usually little change in blood pressure or heart rate occurs. Cardiovascular stability is generally preserved in persons with hypovolemia or cardiac dysfunction.
Etomidate inhibits the enzyme responsible for performing the 11β-hydroxylation reaction in cortisol synthesis. A single induction dose of 0.3 mg/kg inhibits cortisol synthesis and the normal response to adrenocorticotropic hormone for up to 12 hours. Infusions of several days' duration in ventilated intensive care unit patients were associated with increased mortality.
Sedative doses of midazolam cause patients to become sleepy and calmer and to have anterograde amnesia. The amnestic effects of midazolam are variable but usually short-lived, and they should not be relied on to prevent recall of intraoperative events.
Intramuscular administration of midazolam results in reliable absorption and little ...